lncRNA MEG3 increases the radiosensitivity of lung cancer cells by regulating miR-21 / 中华放射肿瘤学杂志
Chinese Journal of Radiation Oncology
; (6): 986-990, 2020.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-868728
Biblioteca responsável:
WPRO
ABSTRACT
Objective:
To investigate the regulatory mechanism of long-chain non-coding RNA (lncRNA) MEG3 on the sensitivity of lung cancer cell line H1299 to irradiation.Methods:
The expression of MEG3 and miR-21-5p in lung cancer cell line H1299 was detected by qRT-PCR. Overexpression control group (transfected with pcDNA3.1), MEG3 overexpression group (transfected with pcDNA3.1-MEG3), miR-NC inhibition group (transfected anti-miR-NC), miR-21-5p inhibition group (transfected with anti-miR-21-5p), MEG3 overexpression+ miR-NC overexpression group (co-transfected with pcDNA3.1-MEG3 and miR-NC), MEG3 overexpression+ miR-21-5p overexpression group (co-transfected with pcDNA3.1-MEG3 and miR-21-5p mimics) were all transfected into H1299 cells by liposome method treated with 4 Gy irradiation. Cell survival fraction was detected by colony formation assay. Cell apoptosis was detected by flow cytometry. The binding of MEG3 to miR-21-5p in cells was assessed by dual luciferase reporter assay.Results:
Compared with normal lung epithelial cells, the expression of MEG3 was significantly decreased, whereas the expression of miR-21-5p was significantly increased in the radioresistant lung cancer cells H1299. Overexpression of MEG3 or inhibition of miR-21-5p could promote the apoptosis and enhance the radiosensitivity of H1299 cells. MEG3 could targetedly regulate the expression of miR-21-5p. Overexpression of miR-21-5p could reverse the enhanced radiosensitivity of MEG3 to H1299 cells.Conclusion:
LncRNA MEG3 can enhance the sensitivity of lung cancer cells H1299 to irradiation. The mechanism may be related to targeting miR-21-5p.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Journal of Radiation Oncology
Ano de publicação:
2020
Tipo de documento:
Artigo